Synaptic and paracrine mechanisms at carotid body arterial chemoreceptors
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Mammalian carotid bodies are the main peripheral arterial chemoreceptors, strategically located at the bifurcation of the common carotid artery. When stimulated these receptors initiate compensatory respiratory and cardiovascular reflexes to maintain homeostasis. Thus, in response to low oxygen (hypoxia) or increased CO2/H(+) (acid hypercapnia), chemoreceptor type I cells depolarize and release excitatory neurotransmitters, such as ATP, which stimulate postsynaptic P2X2/3 receptors on afferent nerve terminals. The afferent discharge is shaped by autocrine and paracrine mechanisms involving both excitatory and inhibitory neuromodulators such as adenosine, serotonin (5-HT), GABA and dopamine. Recent evidence suggests that paracrine activation of P2Y2 receptors on adjacent glia-like type II cells may help boost the ATP signal via the opening of pannexin-1 channels. The presence of an inhibitory efferent innervation, mediated by release of nitric oxide, provides additional control of the afferent discharge. The broad array of neuromodulators and their receptors appears to endow the carotid body with a remarkable plasticity, most apparent during natural and pathophysiological conditions associated with chronic sustained and intermittent hypoxia.
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